Clinical Features

The clinical presentation of TCA toxicity varies tremendously from mild antimuscarinic symptoms to severe cardiotoxicity secondary to sodium channel blockade. In up to 70 percent of TCA poisonings, coingested drugs also are involved, and the additional toxicity from these coingestants should be considered when evaluating these patients. Antimuscarinic symptoms commonly serve as markers for TCA toxicity (e.g., dry mouth and axillae, sinus tachycardia), but they alone are rarely responsible for patient fatalities. Moreover, antimuscarinic symptoms are not uniformly present in TCA toxicity. As an example, sinus tachycardia is the most frequent dysrhythmia noted in TCA toxicity, but it is only present in approximately 70 percent of symptomatic patients. Altered mental status is the most common symptom reported following TCA exposure.

Mild to moderate TCA toxicity may present as drowsiness, confusion, slurred speech, ataxia, dry mucous membranes and axilla, sinus tachycardia, urinary retention, myoclonus, and hyperreflexia. Antimuscarinic syndrome is classically associated with decreased bowel tones and ileus. However, bowel function is fairly resistant to inhibition and active bowel sounds can be present even in seriously ill patients. Therefore, the presence of active bowel tones does not rule out the possibility of antimuscarinic syndrome. Mild hypertension is observed occasionally and rarely requires treatment. Nontolerant individuals occasionally develop coma and respiratory depression after relatively small overdoses without obvious peripheral antimuscarinic effects and without QRS widening. Overflow urinary incontinence may be mistaken for normal micturition in pediatric (diaper-dependent) patients.

Serious toxicity is almost always seen within 6 h of major TCA ingestion and consists of the following symptoms: coma, cardiac conduction delays, supraventricular tachycardia, hypotension, respiratory depression, premature ventricular beats, ventricular tachycardia, and seizures. 8 Secondary complications from serious toxicity include aspiration pneumonia, anoxic encephalopathy, hyperthermia, and rhabdomyolysis. Pulmonary edema is a well-recognized complication of TCA overdose. Seizures are usually generalized and brief in duration. The exception to this rule is seen in amoxapine and maprotiline overdoses. These agents can cause status epilepticus. Amoxapine seizures commonly occur without corresponding QRS widening.

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